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High-intensity sprint training inhibits mitochondrial respiration through aconitase inactivation
Swedish Sch Sport & Hlth Sci, Stockholm, Sweden.
Karolinska Inst, Dept Physiol & Pharmacol, SE-17177 Stockholm, Sweden.
Univ Southern Denmark, Inst Sports Sci & Clin Biomech, Muscle Res Cluster, Odense, Denmark.
Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Univ Wurzburg, Dept Sport Sci, D-97070 Wurzburg, Germany. (NVC)
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2016 (English)In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 30, no 1, p. 417-427Article in journal (Refereed) Published
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Abstract [en]

Intense exercise training is a powerful stimulus that activates mitochondrial biogenesis pathways and thus increases mitochondrial density and oxidative capacity. Moderate levels of reactive oxygen species (ROS) during exercise are considered vital in the adaptive response, but high ROS production is a serious threat to cellular homeostasis. Although biochemical markers of the transition from adaptive to maladaptive ROS stress are lacking, it is likely mediated by redox sensitive enzymes involved in oxidative metabolism. One potential enzyme mediating such redox sensitivity is the citric acid cycle enzyme aconitase. In this study, we examined biopsy specimens of vastus lateralis and triceps brachii in healthy volunteers, together with primary human myotubes. An intense exercise regimen inactivated aconitase by 55-72%, resulting in inhibition of mitochondrial respiration by 50-65%. In the vastus, the mitochondrial dysfunction was compensated for by a 15-72% increase in mitochondrial proteins, whereas H2O2 emission was unchanged. In parallel with the inactivation of aconitase, the intermediary metabolite citrate accumulated and played an integral part in cellular protection against oxidative stress. In contrast, the triceps failed to increase mitochondrial density, and citrate did not accumulate. Instead, mitochondrial H2O2 emission was decreased to 40% of the pretraining levels, together with a 6-fold increase in protein abundance of catalase. In this study, a novel mitochondrial stress response was highlighted where accumulation of citrate acted to preserve the redox status of the cell during periods of intense exercise.

Place, publisher, year, edition, pages
2016. Vol. 30, no 1, p. 417-427
Keywords [en]
exercise, mitochondrial dysfunction, reactive oxygen species, citrate
National Category
Sport and Fitness Sciences
Identifiers
URN: urn:nbn:se:miun:diva-27824DOI: 10.1096/fj.15-276857ISI: 000367621000039PubMedID: 26452378Scopus ID: 2-s2.0-84973472750OAI: oai:DiVA.org:miun-27824DiVA, id: diva2:934072
Available from: 2016-06-08 Created: 2016-06-07 Last updated: 2017-08-09Bibliographically approved

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Zinner, ChristophWillis, Sarah J.Holmberg, Hans-Christer

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